Ultra-low-dose spectral-detector computed tomography for the accurate quantification of pulmonary nodules: an anthropomorphic chest phantom study.

PURPOSE: To assess the quantification accuracy of pulmonary nodules using virtual monoenergetic images (VMIs) derived from spectral-detector computed tomography (CT) under an ultra-low-dose scan protocol. METHODS: A chest phantom consisting of 12 pulmonary nodules was scanned using spectral-detector CT at 100 kVp/10 mAs, 100 kVp/20 mAs, 120 kVp/10 mAs, and 120 kVp/30 mAs. Each scanning protocol was repeated three times. Each CT scan was reconstructed utilizing filtered back projection, hybrid iterative reconstruction, iterative model reconstruction (IMR), and VMIs of 40-100 keV. The signal-to-noise ratio and air noise of images, absolute differences, and absolute percentage measurement errors (APEs) of the diameter, density, and volume of the four scan protocols and ten reconstruction images were compared. RESULTS: With each fixed reconstruction image, the four scanning protocols exhibited no significant differences in APEs for diameter and density (all P > 0.05). Of the four scan protocols and ten reconstruction images, APEs for nodule volume had no significant differences (all P > 0.05). At 100 kVp/10 mAs, APEs for density using IMR were the lowest (APE-mean: 6.69), but no significant difference was detected between VMIs at 50 keV (APE-mean: 11.69) and IMR (P = 0.666). In the subgroup analysis, at 100 kVp/10 mAs, there were no significant differences between VMIs at 50 keV and IMR in diameter and density (all P > 0.05). The radiation dose at 100 kVp/10 mAs was reduced by 77.8% compared with that at 120 kVp/30 mAs. CONCLUSION: Compared with IMR, reconstruction at 100 kVp/10 mAs and 50 keV provides a more accurate quantification of pulmonary nodules, and the radiation dose is reduced by 77.8% compared with that at 120 kVp/30 mAs, demonstrating great potential for ultra-low-dose spectral-detector CT.

Wogonin Restrains the Malignant Progression of Lung Cancer Through Modulating MMP1 and PI3K/AKT Signaling Pathway.

BACKGROUND: Wogonin, a natural flavonoid compound, represses cancer cell growth and induces cancer cell apoptosis in diverse malignancies. However, the function of Wogonin in lung cancer cells and its regulatory mechanism deserve to be identified. METHODS: A549 and H460 cells were treated with Wogonin, and the cell growth, apoptosis, migration and invasion were measured by CCK-8 and EdU, flow cytometry and Transwell assays. The targeted genes of Wogonin and lung cancer were identified from the TCMSP and Genecards databases, respectively. The STRING database and Cytoscape software were used to establish a PPI network and screen hub genes. GO and KEGG analysis was conducted to explore the functions and signal pathways related to the hub genes. MMP1 expression in lung cancer was analyzed using the UALCAN databases, and GSEA was performed utilizing LinkedOmics. Gelatin zymography assay was used to detect MMP1 activity. MMP1 mRNA expression was detected by qRT-PCR. Besides, MMP1, p-AKT and c-Myc protein were detected by Western Blot assay. RESULTS: Wogonin could suppress the proliferation, migration and invasion of A549 and H460 cells and induce apoptosis. GO and KEGG enrichment analysis revealed the hub genes were mostly enriched in re-entry into the mitotic cell cycle and apoptosis. The expression of MMP1 was markedly upregulated in lung squamous cell carcinoma, lung adenocarcinoma tissues, and lung cancer cell lines. Wogonin could significantly inhibit MMP1 expression and activity, and overexpression of MMP1 significantly reversed the effect of Wogonin on the malignant phenotypes of A549 and H460 cells. Wogonin inhibited the expression of p-AKT and c-Myc protein by regulating MMP1. CONCLUSION: Wogonin can repress lung cancer cells' growth and metastatic potential and promote cell apoptosis via repressing MMP1 expression and modulating PI3K/AKT signaling pathway.

Long noncoding RNA regulatory factor X3- antisense RNA 1 promotes non-small cell lung cancer via the microRNA-577/signal transducer and activator of transcription 3 axis.

Lung cancer is the most frequent malignancy, and non-small cell lung cancer (NSCLC) is its most common pathological type. Molecular targeted therapy has been testified to be effective in intervening in the occurrence and development of malignancies. This study investigates the effect of lncRNA Regulatory Factor X3- antisense RNA 1 (RFX3-AS1) in NSCLC progression. The RFX3-AS1 profile in NSCLC tissues and cells was measured by quantitative reverse transcription PCR (qRT-PCR). The RFX3-AS1 overexpression model was constructed. The cell counting kit-8 (CCK-8) experiment and cell colony formation assay were adopted to test cell viability. The cell apoptosis was determined by flow cytometry (FCM). Cell migration and invasion were monitored by the Transwell assay, and Western blot was implemented to verify the protein profiles of signal transducer and activator of transcription 3 (STAT3), E-cadherin, Vimentin and N-cadherin. In vivo, we validated the impact of RFX3-AS1 overexpression on the NSCLC xenograft mouse model. The targeting relationships between RFX3-AS1 and miR-577, miR-577 and STAT3 were confirmed by the dual-luciferase reporter assay. The results manifested that overexpressing RFX3-AS1 markedly facilitated NSCLC cell proliferation, migration, invasion and epithelial-mesenchymal transition (EMT), and suppressed cell apoptosis. In contrast, miR-577, which was a downstream target of RFX3-AS1, dramatically impeded the malignant biological behaviors of NSCLC cells. STAT3 was a direct target of miR-577, and it was negatively regulated by the latter. STAT3 activation reversed miR-577-mediated anti-tumor roles. In brief, RFX3-AS1 aggravated NSCLC progression by regulating the miR-577/STAT3 axis.

Evaluating the impact of personalized rehabilitation nursing intervention on postoperative recovery of respiratory function among thoracic surgery intensive care unit patients: A protocol for systematic review and meta-analysis.

BACKGROUND: Exercise tolerance and lung function can be improved by pulmonary rehabilitation. As a result, it may lower thoracic surgery intensive care unit (ICU) patients' postoperative problems and death. Enhanced recovery after surgery has advanced significantly in the perioperative care of thoracic surgery ICU patients in recent years, and it now plays an essential role in improving ICU patients' postoperative prognosis. Appropriate tailored rehabilitation nursing intervention is required to promote the postoperative recovery of respiratory function in thoracic surgery ICU patients. This study aims to look at the influence of tailored rehabilitation nurse intervention on postoperative respiratory function recovery in thoracic surgery ICU patients. METHODS: To find relevant papers, a comprehensive search of electronic databases will be conducted, including three English databases (PubMed, EMBASE, and the Cochrane Library) and two Chinese databases (Chinese National Knowledge Infrastructure and WanFang). Only research that has been published in either English or Chinese will be considered. The retrieval period will run from November 2021 to November 2021. We will look at randomized controlled trials (RCTs) studies that looked at the effect of a customized rehabilitation nursing intervention on the recovery of respiratory function in thoracic surgery ICU patients after surgery. Two writers will review the literature, retrieve study data, and assess the included studies' quality. Any disagreements will be settled via consensus. RevMan 5.3 will be used to do the meta-analysis. RESULTS: This research will offer high-quality data on the influence of customized rehabilitation nurse intervention on postoperative respiratory function recovery in thoracic surgery ICU patients. CONCLUSION: This study will look at whether a targeted rehabilitation nurse intervention might help thoracic surgery ICU patients recover their respiratory function more quickly after surgery. ETHICS AND DISSEMINATION: There will be no need for ethical approval. REGISTRATION NUMBER: December 12, 2021.osf.io/9rdu2/ (https://osf.io/9rdu2/).

[Advances in bacterial Rieske non-heme iron ring-hydroxylating dioxygenases that initiate polycyclic aromatic hydrocarbons degradation].

Polycyclic aromatic hydrocarbons (PAHs) are a class of persistent organic pollutants, which have received widespread attentions due to their carcinogenic and mutagenic toxicity. The microbial degradation of PAHs are usually started from the hydroxylation, followed by dehydrogenation, ring cleavage and step-by-step removal of branched chains, and finally mineralized by the tricarboxylic acid cycle. Rieske type non-heme iron aromatic ring-hydroxylating dioxygenases (RHOs) or cytochrome P450 oxidases are responsible for the conversion of hydrophobic PAHs into hydrophilic derivatives by the ring hydroxylation. The ring hydroxylation is the first step of PAHs degradation and also one of the rate-limiting steps. Here, we review the distribution, substrate specificity, and substrate recognition mechanisms of RHOs, along with some techniques and methods used for the research of RHOs and PAHs.

Nek9,a sensitive immunohistochemical marker for Schwannian, melanocytic and myogenic tumours.

AIMS: In our previous study, striking Nek9 staining was observed in peripheral nerves for the first time. Therefore, in the current study, we aimed to detect Nek9 expression in peripheral nerve sheath tumours, melanocytic tumours and their mimics. METHODS: The expression of Nek9 was analysed in 234 mesenchymal tumours including schwannoma, neurofibroma, malignant peripheral nerve sheath tumour (MPNST), melanoma and their mimics adopting immunohistochemistry. In addition, S-100 and SOX10 were detected in all tumours. RESULTS: The results revealed an intense and diffuse staining of Nek9 in all schwannomas (30/30) and melanomas (20/20). The neurofibromas (86%, 19/22) and MPNSTs (76%, 18/21) showed a high frequency of positive Nek9 staining. Nek9 showed a comparable sensitivity to S-100, and better sensitivity and less specificity than that of SOX10. Among the histological mimics, Nek9 was only strongly and diffusely expressed in rhabdomyosarcomas (RSs) (97%,37/38) while negatively stained in most of the other tumours. It was noted that Nek9 immunoresponse was more diffuse than that of MyoD1 and myogenin in RS. CONCLUSIONS: In summary, Nek9 has a good sensitivity in the diagnosis of tumours with Schwannian, melanocytic and skeletal muscle differentiations. The immunohistochemical analysis of Nek9 expression may be helpful in the diagnosis and differential diagnosis of the aforementioned tumours.

[Real-time cell analysis combined with pattern recognition to evaluate anaphylaxis of Zushima Injection].

This paper was aimed to establish a new method for evaluating the anaphylactoid reaction of 15 batches of Zushima Injection from different manufacturers in vitro. Basophilic leukemia cell line RBL-2 H3 cells were cultured in vitro and Compound 48/80 was selected as positive drug. Real-time cell analysis(RTCA) system was used to detect the changes of cell index(CI) value after drug intervention. The degranulation of RBL-2 H3 cells was verified with the toluidine blue staining technology by observing the changes of cell morphology and skeleton. Clustering method was used to analyze the CI values of 15 batches of Zushima Injection on RBL-2 H3 cells. The results showed Compound 48/80(20 µg·mL~(-1)) significantly changed the cell morphology and cytoskeleton, with obvious degranulation. After adding Compound 48/80, CI value decreased rapidly within 30 minutes, then decreased slowly, suggesting that RTCA system can be used for rapid and sensitive evaluation of RBL-2 H3 cell degranulation. The results of cluster analysis showed that Zushima Injection from different manufacturers had different effects on RBL-2 H3 cells. S1-S8 and Compound 48/80 groups were grouped into one cluster, which suggesting that the sample might have potential clinical anaphylaxis. S9-S15 and the normal control group were grouped into one cluster, suggesting there was no anaphylactoid reaction in the sample. In this study, a rapid in vitro anaphylaxis evaluation technique based on RTCA system and pattern recognition method was established, which can be used for rapid in vitro evaluation of anaphylaxis for traditional Chinese medicine injection.

Cyclin-dependent kinase subunit 2 overexpression promotes tumor progression and predicts poor prognosis in uterine leiomyosarcoma.

Cyclin-dependent kinase subunit (CKS) 2 is a member of the CKS family, which plays an important role in the regulation of meiosis and mitosis. Overexpression of CKS2 has been reported in several types of tumors. However, few studies have investigated its role in uterine leiomyosarcoma (ULMS). In the present study, the expression of CKS2 in 38 cases of ULMS and 38 cases of uterine leiomyoma (ULM) was analyzed by immunohistochemistry. Moreover, the functional analysis of CKS2 was performed in ULMS cell lines. A significantly higher expression of CKS2 was found in ULMS tissues than in ULM tissues (P<0.01) and high CKS2 expression was associated with increased tumor size, low progesterone receptor expression and poor prognosis in patients with ULMS. Multivariate Cox regression analysis revealed that CKS2 expression status was an independent predictor of overall survival for ULMS. Furthermore, silencing of CKS2 in ULMS cells inhibited cell proliferation, colony formation, migration and invasion, and resulted in cell cycle arrest. In conclusion, the present study demonstrated that CKS2 may serve as a marker for the differential diagnosis of ULMS and ULM. In addition, it may act as an independent prognostic factor in patients with ULMS, and serve as a novel target for ULMS therapy.

Contrast optimization in broadband passive polarimetric imaging based on color camera.

Broadband polarimetric imaging consists of forming an image under spectrally wide illumination after having optimized the polarization state analyzer (PSA) to maximize the target/background discriminability. In previous works, the image sensor was monochrome, and only the intensity contrast was optimized. However, due to its spectrally varying response, the PSA not only changes the light's intensity, but also its color. This color information can serve as a further parameter to improve discrimination. In this paper, we employ a color camera in a broadband Stokes (passive) polarimetric imaging system and take into color difference's contribution to discrimination ability in optimizing the PSA setting. We show through experiments that a significant improvement of discrimination ability over monochrome imaging is obtained, especially when there are multiple objects in the scene.

Optimal ellipsometric parameter measurement strategies based on four intensity measurements in presence of additive Gaussian and Poisson noise.

The two ellipsometric parameters of an isotropic sample can be measured with simplified polarimetry setups that acquire at least four intensity measurements. However, these measurements are perturbed by noise and the measurement strategy has to be optimized, in order to limit noise propagation. We determine two different measurement strategies that are optimal for both white Gaussian additive noise and Poisson shot noise. The first one involves a polarization state generator (PSG) with a single state of polarization and a polarization state analyzer (PSA) with four states. The second one involves both PSG and PSA having two states. The total estimation variances obtained with both strategies are demonstrated to be minimal, of equal values, and independent of the ellipsometric parameters to be measured. They are based on simple optical elements and could simplify and accelerate ellipsometric measurements.

The expression of microRNA-324-3p as a tumor suppressor in nasopharyngeal carcinoma and its clinical significance.

OBJECTIVE: This study aimed to determine the expression, clinical significance, and possible biologic function of microRNA-324-3p in nasopharyngeal carcinoma (NPC) tissues. METHODS: In total, 54 NPC and 35 control tissues were collected. The correlation between miR-324-3p expression and the clinicopathologic characteristics was analyzed. A dual-luciferase reporter gene assay was employed to examine the predicted target gene of miR-324-3p. The miR-324-3p expression level in 5-8F cells was determined with quantitative reverse transcription-polymerase chain reaction following the transfection of miR-324-3p mimics and inhibitors. Cell proliferation and the percentage of apoptosis were measured with MTT and flow cytometry. Cell invasion ability was assessed by Transwell invasion assay. RESULTS: Our results showed that miR-324-3p was downregulated in the NPC tissues. The expression level of miR-324-3p in poorly differentiated NPC was significantly reduced in comparison with that in well/moderately differentiated NPC. The expression level in clinical stages III/IV was lower than that in clinical stages I/II. Moreover, the expression level of miR-324-3p was significantly lower in NPC patients with lymph node metastasis than that in NPC patients without lymph node metastasis. NPC patients with higher levels of miR-324-3p expression also demonstrated a longer survival time. Predictions from bioinformatics indicated the Hedgehog pathway transcription gene GLI3 as the target gene of miR-324-3p, and the dual- luciferase reporter assay showed that miR-324-3p is directly combined with the 3'-untranslated region of GLI3. The overexpression of miR-324-3p suppressed cell proliferation and invasion, and it enhanced apoptosis in 5-8F cells. CONCLUSION: miR-324-3p can act as a tumor suppressor in NPC cells by the negative regula- tion of GLI3 gene.

ANRIL is associated with the survival rate of patients with colorectal cancer, and affects cell migration and invasion in vitro.

Antisense noncoding RNA in the INK4 locus (ANRIL) has been reported to be upregulated in various types of human cancer, and is also highly expressed in normal human tissue. The aim of the present study was to identify whether ANRIL may be a possible target for colorectal cancer (CRC) therapy. Reverse transcription­quantitative polymerase chain reaction was used to quantify the expression levels of the long noncoding RNA (lncRNA) ANRIL in 97 paired CRC and adjacent non­neoplastic tissue samples. In addition, the HT29 and RKO human CRC cell lines underwent ANRIL RNA interference, and knockdown efficiency was evaluated by western blotting. Cell viability, and migratory and invasive ability were subsequently assessed. The CRC tissues were revealed to express higher levels of ANRIL lncRNA compared with the adjacent non­neoplastic tissues (P<0.05). Furthermore, high ANRIL expression was significantly associated with reduced survival rate (P<0.05). ANRIL gene expression was successfully silenced in human CRC cells. ANRIL knockdown decreased proliferation, inhibited migration and invasion, and reduced the colony­forming ability of the cells. These data indicated that the lncRNA ANRIL is upregulated in CRC tissues, and is associated with CRC cell pathogenesis. Furthermore, the underlying mechanisms of these effects may be exploited for therapeutic benefit.

Knockdown of microRNA-1323 restores sensitivity to radiation by suppression of PRKDC activity in radiation-resistant lung cancer cells.

Resistance to radiation is a major problem in cancer treatment. The mechanisms of radioresistance remain poorly understood; however, mounting evidence supports a role for microRNAs (miRNAs) in the modulation of key cellular pathways mediating the response to radiation. The present study aimed to identify specific miRNAs and their effect on radioresistant cells. The global miRNA profile of an established radioresistant lung cancer cell line and the corresponding control cells was determined. Differential expression of the miRNAs was confirmed by quantitative real-time PCR (qRT-PCR). The binding effect of identical novel miRNAs and target mRNAs was determined by luciferase assay. Lung cancer cells were transfected with miRNA-specific mimics or inhibitors. The DNA-dependent protein kinase (DNA-PKcs) protein level was tested by western blot analysis. Radiosensitivity of cancer cells was determined using colony formation assay. Among the differentially expressed miRNAs, 25 miRNAs were overexpressed while 18 were suppressed in the radioresistant cells, both basally and in response to radiation compared to their control. An miRNA signature miR-1323 exhibited a >5-fold increase in the radioresistant cells. miR-1323 was demonstrated to bind to PRKDC 3'UTR, which is involved in DNA repair. Ectopic expression of miR-1323 significantly increased the survival fraction of irradiated cancer cells. Inhibition of miR-1323 reversed the radioresistance of cancer cells and subsequently suppressed the expression of miR-1323-regulated DNA-PKcs protein. The present study indicated that miRNAs are involved in the radioresistance of human lung cancer cells. A possible mechanism for resistance to radiation was via enhanced DNA repair. The present study demonstrated a role for miR-1323 in modulating radioresistance and highlights the need for further study investigating the potential role of miR-1323 as both a predictive marker of response and a novel therapeutic agent with which to enhance the efficacy of radiotherapy.

Radio frequency interrogated actively mode-locked fiber ring laser for sensing application.

This paper proposes an actively mode-locked fiber ring laser for sensing applications. Mode-locking of the laser is achieved by driving an electro-optic amplitude modulator at an RF corresponding to the fundamental beat frequency between the longitudinal modes. The change of the cavity length produces a frequency comb around the beat frequencies. The frequency separation of the comb is found to be linearly proportional to the cavity length change. The sensing mechanism of the device is shown. Temperature measurement is demonstrated using the proposed actively mode-locked fiber ring laser.

Optical fiber sensor based on a radio frequency Mach-Zehnder interferometer.

This Letter proposes an optical fiber radio frequency (RF) Mach-Zehnder interferometer (MZI) for sensing applications. An RF modulated laser source is injected into an optical fiber RF-MZI and collected by a photodiode. The interference pattern is observed in the RF domain by sweeping the frequency using a network analyzer. The proposed sensor has a linear response to applied temperature change. In addition, the sensitivity, observation frequency range, and the length of the sensing arm are discussed.

[Effects of granulocyte colony-stimulating factor on hepatocyte apoptosis in acute liver failure: experiment with rats].

OBJECTIVE: To explore the effects of granulocyte colony- stimulating factor (G-CSF) on hepatocyte apoptosis in acute liver failure (ALF) and possible mechanism thereof. METHODS: One hundred and sixty SD rats underwent intraperitoneal injection of D-galactosamine (D-GalN) 1.4 g/kg so as to establish AFL models and then were randomly divided into 2 equal groups: G-CSF therapy group, injected hypodermically with recombinant human G-CSF 50 microg x kg(-1) x d(-1) 2 hours after D-GalN injection for 3 consecutive days, and placebo control group, injected hypodermically with normal saline for 3 consecutive days. Liver samples were collected from 6 rats of each group 6 h, 12 h, 1 day, and 3 days after D-GalN injection respectively. Another six normal rats were used as normal control group. Hepatocyte apoptosis rate was measured by flow cytometry. Immunohistochemistry was used to detect the expression of Bcl-2 and caspase-3, a proapoptosis protein, in the liver sections. RESULTS: The survival rate of the G-CSF therapy group was 53.3%, significantly higher than that of the placebo control group (33.3%, P = 0.027). The hepatocyte apoptosis rate and expression rates of Bcl-2 and caspase-3 in the liver sections after D-GalN injection increased along with time. The hepatocyte apoptosis rate peaked 1 day after the D-GalN injection in both groups. The maximum hepatocyte apoptosis rate of the G-CSF group was 29% +/- 7%, significantly lower than that of the placebo control group (44% +/- 12%, P = 0.026). The gray scale of Bcl-2 in liver sections at hour 12 of the G-CSF group was 152 +/- 37, significantly lower than that of the placebo control group (161 +/- 7, P = 0.012). and the gray scale of Bcl-2 on day 1 of the G-CSF group was 150 +/- 12, significantly lower than that of the placebo control group (159 +/- 9, P = 0.018). The gray scales of caspase-3 on days 1 and 3 of the G-CSF group were 189.6 +/- 4.6 and 184.7 +/- 4.8 respectively, both significantly higher than those of the placebo control group (169.6 +/- 15.7 and 160.0 +/- 5.0, both P = 0.000). CONCLUSION: Apoptosis is a key mechanism contributing to ALF. G-CSF prevents ALF induced by D-GalN, thus raising the survival rate. G-GSF shows an inhibitory efficacy on hepatocytes apoptosis by probably up-regulating Bcl-2 and reducing caspase-3 expression.

Correlation of serum leptin levels with anthropometric and metabolic parameters and biochemical liver function in Chinese patients with chronic hepatitis C virus infection.

AIM: To determine serum leptin levels and investigate their correlations with anthropometric and metabolic parameters and biochemical liver function in patients with chronic hepatitis C virus (HCV) infection and their potential clinical implications. METHODS: Forty-two chronic HCV-infected patients without anti-viral treatment were enrolled in this study, 30 patients had chronic hepatitis C, 10 had cirrhosis, and 2 had hepatocellular carcinoma (HCC). Thirty age- and sex-matched healthy individuals served as controls. Serum leptin levels were determined by ELISA. The biochemical liver function and serum lipids were determined at the same time. The height and body weight of patients and controls were measured, and body mass index (BMI) and body fat were calculated simultaneously. The correlations of serum leptin levels with anthropometric and metabolic parameters and biochemical liver function were assessed statistically. RESULTS: The mean of serum leptin levels in patients with chronic hepatitis C, HCV-associated cirrhosis, HCV-associated HCC and control groups was (6.13+/-3.94), (5.25+/-4.21), (4.17+/-0.28), and (3.59+/-3.44) ng/mL, respectively. The serum leptin level in patients with chronic hepatitis C was significantly higher than that in controls. The serum leptin levels between cirrhotic patients and controls and between male and female cirrhotic patients had no significant difference. Serum leptin levels were positively-correlated with body fat, BMI, and apolipoprotein B (Apo B) in patients with chronic HCV infection. The serum alanine aminotransferase (ALT) levels were closely-correlated with BMI in patients with chronic hepatitis C. CONCLUSION: HCV infection interferes with fat and lipid metabolism in patients with chronic HCV infection and leptin may play a role in hepatosteatosis.